Assignment of the canalicular mlltiorganic anion transporter (cMOAT) gene to human chromosome 10q24 and mouse chromosome 19D2

M. A. Van Kuijck, G. F.M. Merkx, M. Kool, A. Geurts Van Kessel, R. J.M. Bindeis, P. M.T. Deen, C. H. Van Os

Research output: Contribution to journalArticlepeer-review

Abstract

Recently, we isolated a rabbit cDNA which encodes a novel member of the ATP-binding cassette (ABC) superfamily of transporters. In Xenopus laevis oocytes expressing this protein, a cAMP-activated chloride conductance was demonstrated. This protein was, therefore, baptized epithelial basolateral chloride conductance regulator (Ebcr). At the same time, a rat liver ABC transporter, named cMoat, was identified, which appeared to be absent in TR- rats. These rats are used as a model for Dubin-Johnson syndrome (DJs) in humans, which is a congenital form of jaundice. Comparison of Ebcr and cMoat amino acid sequences showed 78.5% identity. Furthermore, we elicited by Northern blot analysis that Ebcr and cMoat labeled fragments as probes, detect in several rabbit tissues only one transcript, which is of identical size and relative abundance. It is thus very likely that Ebcr is the homologue of rat cMoat. In order to be able to couple diseases like DJs to cMOAT dysfunctioning, chromosomal localization of human cMOAT is essential. Using fluorescent in situ hybridization, the cMOAT gene was assigned to human chromosome 10q24 and mouse chromosome 19D2.

Original languageEnglish
Pages (from-to)A26
JournalFASEB Journal
Volume11
Issue number3
Publication statusPublished - 1997
Externally publishedYes

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